Of the ~4 million pregnant women each year, insomnia and pregnancy-related sleep disturbances plague
upwards of 50-60% (> 2 million women) by the third trimester. Pregnancy can initiate and exacerbate insomnia
symptoms that often extend into the postpartum period. In fact, rates as high as 41% have been reported up to 2
years postpartum. Despite this pervasiveness, insomnia is often considered a transient symptom of childbearing
with few consequences for mental or physical health. As a result of this thinking, there have been few studies
examining the impact of insomnia on pregnancy/postpartum maternal mental or physical health, well-being or
infant outcomes. This is in spite of the fact that insomnia and emerging phenotypes (i.e., with short sleep
duration) appear to increase depressive symptomatology and dysregulate immune and hypothalamic-pituitary-
adrenal axis (HPA) activity. Each of which may subsequently translate into adverse maternal morbidities, such
as gestational hypertension or diabetes, or poor outcomes, including preterm birth. Moreover, given the known
long-term consequences of maternal morbidity on infant mental and physical health, the need to examine these
associations longitudinally is sorely needed. So, one objective of this R15 proposal is to obtain preliminary data
regarding the frequency of various insomnia phenotypes, and examine how they are correlated with recurrent
depressive symptomology, immune, and HPA axis activity among perinatal women with a history of PPD. We
will also explore the role of fetal sex on infant HPA activity and how it is modified by insomnia (phenotypes). The
second objective of this AREA proposal is to expose both graduate and undergraduate students to biomedical
research. A sample of 100 pregnant women (18-45 years of age) between 16-20 weeks gestation will be recruited,
with reassessment at 28-31 weeks and at 3 months postpartum (along with their infant) to address the following
aims. AIM 1: To assess the degree of recurrent depressive symptomatology and physiological dysregulation
among four groups of pregnant and postpartum women. 1) insomnia with short sleep duration (ISQ+ + < 6
hours via actigraphy); 2) insomnia with normal sleep duration (ISQ+ + ≥ 6 hours); 3) short sleepers & no insomnia
(ISQ- and ≥ 6 hours); and 4) healthy sleepers (ISQ- and normal sleep duration ≥ 6 hours). AIM 2: To assess the
extent that physiological dysregulation mediates the association between insomnia and depressive
symptomatology during pregnancy and postpartum. Physiological dysregulation will be assessed by immune
markers (IL-4, IL-6, IL-8, IL-10 and TNF-α) and HPA axis activity (diurnal release of cortisol, CAR, and slope).
Exploratory Aims: (1) To assess whether insomnia, depression and physiological dysregulation during pregnancy
is modified by fetal sex. (2) Explore the amount of infant HPA axis dysregulation among the four maternal
insomnia groups. We anticipate that perinatal women with insomnia and short sleep duration will have greater
depressive symptoms and physiological dysregulation than the other three groups. Also, we expect physiological
dysregulation will mediate the association between insomnia and depression.